Implications of ischemic penumbra for the diagnosis of brain death:
Apnea testing may induce rather than diagnose death 

Introduction

Current diagnosis of brain death may exclusively rely on testing for synaptic activity of brain tissue for a few hours. A 10-min. apnea testing usually follows clinical examination demonstrating absence of brain stem reflexes in a deeply comatose patient - Glasgow Coma Scale (GCS) score of 3. A flat electroencephalogram (EEG) may ultimately confirm brain death for procurement of transplantable organs. Therefore, the overall absence of neurologic function for usually 6 hours has been regarded as a consequence of irreversible whole brain or brain stem damage.

Since Harvard Ad Hoc Commission redefined death as brain death ¹ the period advised for monitoring neurological status has been decreased from 24 to 6 hours ² and, more recently, not required at all ³. Furthermore, apnea testing has been extended to 10 min., and associated with hyperbaric pre-oxygenation and intra-testing "passive oxygenation" through an endotracheal catheter ³. Other confirmatory tests have been proposed alternatively to EEG or angiography, but the reliability of neurological examination and apnea testing has been most considered, up to the point of regarding brain death as "a clinical diagnosis" ³.

Through the last 30 years, validation of diagnostic criteria for brain death has relied on the assumption that inactive brain functions on clinical testing reflects intracranial circulatory arrest resulting from maximally increased intracranial pressure ⁴. Accordingly, absence of intracranial vascular images on cerebral angiography has long been suggested as a confirmatory sign of brain death ^{5, 6}. Recently, a new Brazilian law based on presumed consent for organ donation has raised discussions concerning the reliability of diagnosis of brain death. This text is intended to advance such controversy to the international level, by discussing the implications of ischemic penumbra to the diagnosis of irreversible brain damage and intracranial circulatory arrest.